DEFINITION

Autologous chondrocyte implantation (ACI) was first described by Brittberg et al2 in 1994 in which articular cartilage is harvested, enzymatically prepared to isolated chondrocytes, cultured to undergo proliferation, and transplanted into an articular cartilage defect to produce “hyaline-like” cartilage.

Browne and Branch3 divided articular cartilage surgical options into reparative and restorative categories. Reparative procedures, such as microfracture, although efficacious in some clinical studies, result in primarily a fibrocartilage repair tissue. Restorative procedures, such as osteochondral autograft transfer and ACI, result in repair tissue with higher concentrations of chondrogenic cells and type II collagen present in native articular cartilage. ACI preserves the subchondral plate below the articular cartilage, whereas microfracture disrupts this native architecture.

ACI is performed as a two-stage procedure (FIG 1). In the first stage, articular cartilage is biopsied from the periphery of the femoral condyle either medial or lateral. The cells are then cultured and subsequently reimplanted during the second stage. First-generation ACI uses a periosteal patch sutured over the defect that serves to contain the cells. This technique has resulted in an elevated reoperation incidence typically due to periosteal patch hypertrophy with rates up to 50%.1,8,10,14,17 Second- and third-generation ACI has been described using a collagen membrane (C-ACI) and membrane-associated

(MACI) techniques.8,15,22,23,26 These newer generation techniques result in less morbidity due to avoidance of periosteal patch harvest and graft hypertrophy rates as low as 5%.8

 

 

 

FIG 1 • Overview of the ACI technique. Step 1: Articular cartilage cells are harvested. Step 2: Cells are grown in culture for 4 to 6 weeks. Step 3: The lesion is débrided and prepared. Step 4: Harvested periosteum is sutured onto the defect. Step 5: Cultured chondrocyte cells are implanted.

 

 

Currently, MACI is not approved for use in the United States. Collagen membranes are currently considered off-label use for articular cartilage procedures and approved primarily for indications of rotator cuff repair, tendon augmentation procedures, as well as dental applications. Therefore, this chapter will focus on first-generation periosteal patch ACI and C-ACI techniques.

 

ANATOMY

 

 

Knowledge of articular cartilage anatomy is paramount to understanding articular restoration or reparative techniques. Articular cartilage is divided into four distinct zones: superficial, middle, deep, and calcified.3 Articular cartilage is a viscoelastic material made up of chondrocytes (1% to 5%), water (75%), collagen

(10%), and proteoglycans (10%).3,25 Chondrocytes are the primary cell in articular cartilage that originate from

undifferentiated mesenchymal marrow stem cells. The extracellular matrix consists of type II collagen (95%) and smaller amounts of collagen types IV, VI, IX, X, and XII that provide the tensile strength. Chondroitin and keratin sulfate are negatively charged proteoglycans that attract and hold water while providing the compressive strength.

 

Knee articular cartilage varies from 2 to 6 mm in thickness based on peak contact pressures. It is aneural and lacks a vascular or lymphatic supply. Nutritional supply and removal of metabolites are provided by the synovial fluid.

 

Mechanisms of Articular Cartilage Function

 

An understanding of the mechanisms of articular cartilage function is critical to the surgeon's decision-making process when choosing between reparative and restorative procedures for treatment of cartilage injuries.

Without this knowledge, the simpler and easier techniques of cartilage repair may be selected in lieu of the better long-term solutions of articular cartilage restoration. The direction of modern tissue engineering is

directly toward mimicking the tribologic characteristics of native articular cartilage.16

 

There are three main mechanisms for the low-friction properties of articular cartilage. The first mechanism relies on the structural characteristics of the surface of the superficial layer. The lamina splendens has a horizontal mat of type II collagen fibrils which when viewed on electron microscopy is extremely smooth. The cell density within the superficial layer is the greatest and designed to resist the shear forces present during

articulation.7,28

 

 

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The second mechanism involves lubrication of the articular cartilage and can be characterized by fluid film and boundary lubrication. Fluid film lubrication occurs when the two surfaces are separated by the thickness of a

viscous fluid greater than the surface aberrations preventing structure to structure contact.20 Boundary lubrication occurs at the microfilm level where molecules such as phospholipids plant their hydrophobic body

 

toward the articular cartilage and point their hydrophilic tail toward the opposite articular cartilage.19 Finally, “weeping” lubrication may impact articular cartilage friction by releasing interstitial fluid from compressed cartilage, creating a flow effect.13 “Boosted” lubrication may occur, forcing fluid back into the

extracellular matrix, thus increasing lubricant at the joint interface.27 All of these mechanisms for optimizing

articular cartilage friction properties to the lowest possible degree are unlikely to be found in reparative procedures for articular cartilage injuries and have a higher chance of success as surgeons attempt to develop restorative procedures for articular cartilage injuries such as ACI.

 

PATHOGENESIS

 

Articular cartilage injuries most commonly occur in the setting of a traumatic injury to the knee. This may occur via three mechanisms, the first being a direct blow to the chondral surface such as the knee striking the ground during a fall or “dashboard” injury during a motor vehicle accident. The second occurs as a result of a ligamentous injury to the knee in which ligamentous insufficiency results in abnormal translation of the knee with traumatic contact of the chondral surfaces with each other. The third results from a shear injury to the chondral surfaces during a traumatic patella dislocation.

 

Articular cartilage lesions can also occur as the result of more insidious causes such osteochondritis dissecans, osteonecrosis, focal degenerative changes, overload from limb malalignment, infection, and inflammatory arthritis. Lesions as the result of inflammatory arthritis, infection, or bipolar chondral lesions Outerbridge grade III or greater are a contraindication to ACI.

 

It is important for the surgeon to understand the underlying biologic impact of each of these mechanisms as they have different consequences to margins and depths of the articular damage.

 

In a classic paper by Donohue et al,5 a lower energy direct blow to the articular cartilage can cause blistering

of the articular cartilage, with advancement of the tidemark creating a lesion that has minimal effects to the subchondral bone. These injuries are more amenable to restoration through ACI. On the other hand, a higher energy mechanism that causes subchondral fracture such as patellar dislocation creating a fracture or ligament loss that causes larger, irregular surface area lesions with damage to the subchondral bone may be a

less successful candidate.6,11,12

 

NATURAL HISTORY

 

Articular cartilage lesions have a limited capacity to regenerate due to its low mitotic rate, low turnover rate, low cellto-matrix volume, and lack of a vascular supply. Progenitor cells capable of assisting in healing are located below the calcified cartilage, so only injuries that penetrate the subchondral plate have the capacity to

form a fibrin clot with resultant fibrocartilage formation.23 This results in biomechanically inferior tissue to native hyaline cartilage.

 

The natural history of untreated articular cartilage lesions is unknown, and to date, no formal studies have reported the results in a large cohort of patients. The progression of lesions over time is also confounded by factors such as patient age, chronicity of the lesion, limb alignment, activity level, ligamentous stability, body mass index (BMI), and status of the menisci.

 

Relative consensus exists among authors with regard to lesions that are amenable to treatment with ACI. This includes symptomatic lesions Outerbridge grade III or IV, International Cartilage Repair Society (ICRS) grade 3 or 4, lesion size greater than 2 cm2, and patients aged 50 years or younger.4,9,17,23

PATIENT HISTORY AND PHYSICAL FINDINGS

 

Patients with articular cartilage lesions commonly present after a traumatic episode. This may occur in the setting of a concomitant ligament injury such as an anterior cruciate ligament injury during a sporting activity or from a direct impact to the cartilage such as a dashboard injury that occurs during a motor vehicle accident.

Additional traumatic causes may occur in the setting of a patella instability event. Other articular cartilage lesions may present in a more insidious manner such osteochondritis dissecans, focal osteonecrosis, or early focal degenerative changes.

 

Patient history must also include any previous surgical procedures to the knee and complications that may have occurred. If previous surgery has been performed, review of the operative report or images is important to reveal if the subchondral bone was invaded either by the defect itself or as a result of the surgical procedure (ie, débridement, chondroplasty, microfracture, mosaicplasty, scaffold procedure). A history of violation of the subchondral bone has been shown to negatively affect the clinical outcome of ACI by weakening the construct and functioning more as a microfracture procedure producing type I collagen

fibrocartilage.4 The patient can then be counseled on appropriate expectations.

 

Physical examination findings most commonly reveal an effusion, often accompanied by pain and quadriceps inhibition. Mechanical symptoms such as catching and locking may represent a loose body or unstable chondral flap. Palpable tenderness over the affected compartment may be present.

 

Assessment of the knee for standing alignment and range of motion should be performed. A thorough examination of the entire knee to evaluate concomitant pathology to the menisci and knee ligaments is critical to assure all pathology is appropriately documented and treated.

 

When considering ACI, the patient should be questioned for a known history of hypersensitivity to gentamicin or other aminoglycosides because this antibiotic is used in the cartilage biopsy transport media and culture

media during cell processing.4

 

Additional considerations include assessment of patient's BMI; willingness to comply with the extensive, and at times restrictive, rehabilitation program; and smoking status.

 

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

A complete series of plain knee radiographs including standing posteroanterior flexion, notch, tangential patellofemoral, 30- to 45-degree lateral, and long-leg standing

 

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alignment views allow for assessment of joint space, alignment, osseous loose bodies, cystic changes, and osteophyte formation.

 

 

 

 

FIG 2 • T2-weighted MRI mapping of articular cartilage showing (A) normal articular cartilage and (B) degenerated articular cartilage. (Courtesy of Hollis Potter, MD, and Riley Williams, MD, Hospital for Special Surgery, New York, NY.)

 

 

Magnetic resonance imaging (MRI) offers the most detailed modality for clear delineation of articular cartilage lesion size, involvement of subchondral bone, and location. Thin cut proton density imaging and T2-weighted

Concomitant intraarticular cartilage pathology to the menisci and ligaments is also easily visualized.

 

MRI is also useful to assess articular cartilage lesions after a restorative or reparative procedure has been performed to evaluate percent fill of the lesion, integration into the subchondral bone, and articular cartilage quality.

 

More advanced MRI techniques have recently been described to assess articular cartilage lesions.25 Delayed gadolinium-enhanced MRI (dGEMRIC) demonstrates the range of glycosaminoglycan (GAG) distribution in the cartilage. T2 mapping sequences allow for assessment of type II collagen fiber organization within the extra cellular matrix (FIG 2).

 

DIFFERENTIAL DIAGNOSIS

 

 

 

 

 

 

 

Meniscal pathology Unstable chondral flap Loose body Osteochondral fracture Osteochondritis dissecans Osteonecrosis Osteoarthritis

NONOPERATIVE MANAGEMENT

 

Conservative treatment of a symptomatic chondral defect may be considered controversial by some authors secondary to concern for progression of the lesion over time.

 

Activity restrictions with avoidance of impact exercises or occupational exposure decreases the peak forces on the lesion.

 

Patients with an elevated BMI and more chronic lesions may benefit from a weight loss program.

 

Physical therapy can assist in maximizing range of motion, quadriceps strength, and hip/core strength for optimal knee mechanics.

 

Use of an unloader brace may assist patients with limb malalignment.

 

Ice, nonsteroidal anti-inflammatory drugs, and a compressive knee sleeve provide symptomatic relief of the knee with acute pain and effusion.

 

SURGICAL MANAGEMENT

Preoperative Planning

 

Indications for ACI include patients from adolescent age to age 50 years; symptomatic full-thickness unipolar

articular cartilage lesion involving the femoral condyles, trochlea, and patella; and lesion size 2 to 10 cm2 (FIG 3). As previously mentioned, the patient must be willing to comply with the procedure-specific rehabilitation program required postoperatively to maximize biologic healing and clinical result. Anterior one-half tibial plateau lesions may be accessible for ACI, whereas posterior plateau lesions are difficult to address with these techniques.

 

Prior to proceeding with ACI, coexisting knee pathology must be addressed. Correction of ligamentous instability, limb malalignment, meniscal pathology, and/or abnormal patella maltracking should be performed

first. Clinical outcome after ACI is improved when these abnormalities have been corrected.4,9,17,18 The authors routinely perform these procedures at the time of articular cartilage biopsy. Concomitant pathology can be corrected at the same time as ACI, but any additional surgical procedures must be able to accommodate the postoperative range of motion protocol and load restrictions required for ACI procedures.

 

Positioning

 

The patient is supine on the operative table. A thigh tourniquet is placed for control of bleeding. A lateral thigh brace and foot support are used to support the extremity if flexion is required to access the lesion. Regional anesthesia such as a femoral nerve block is used for postoperative pain control.

 

Approach

 

A midline incision is employed most frequently. A medial or lateral arthrotomy is then performed to access the lesion.

 

For some easily accessible lesions, a limited arthrotomy with use of Doane “Z” retractors may allow sufficient exposure.

 

If there are multiple lesions to address or the lesion is far posterior, a more extensive incision may be required.

 

For periosteal patch harvest, a separate 4-cm incision is made distal to the tibial tubercle and pes anserinus tendon insertion on the proximal medial tibia.

 

The authors use a hooded personal protection system, similar to that used in joint arthroplasty, during ACI procedures secondary to proximity to the wound during handling of transplanted tissue and sometimes awkward positioning necessary to suture the graft patch.

 

 

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FIG 3 • Algorithm for treatment of articular cartilage lesions. (From Browne JE, Branch TP. Surgical alternatives for treatment of articular cartilage lesions. J Am Acad Orthop Surg 2000;8[3]:180-189.)

 

TECHNIQUES

• Step 1. Diagnostic Arthroscopy and Articular Cartilage Biopsy

   

  The first stage of the procedure is to perform a thorough diagnostic arthroscopy to document the status of all articular cartilage surfaces, meniscal integrity, and ligamentous stability. The articular cartilage lesion should be carefully probed. The location, depth, and size of the lesion are carefully documented. The ICRS has developed a form (ICRS Cartilage Defect Mapping) that allows for objective mapping of the lesion characteristics (TECH FIG 1A).

   

  If the cartilage defects are deemed amenable to ACI, then harvesting of the articular cartilage biopsy is performed. The most common sites for biopsy include the osteochondral ridge of the superior medial or lateral femoral condyle. These sites are of minimal load bearing and result in the lowest morbidity from harvest. If the patellofemoral joint is the primary site of pathology, then consideration for biopsy from the lateral intercondylar notch is given.

   

  Optimal biopsy volume is 200 to 300 mg for culture. This equates to 2 “tic-tac-sized” biopsy specimens measuring approximately 5 mm wide by 1 cm in length. This biopsy size contains the 200,000 to 300,000 cells that undergo enzymatic digestion, differentiation, and expansion to 9 to 12 million cells per 0.4 mL of

  culture medium per vial.4

   

  The biopsy is best procured using a curved ring curettes (TECH FIG 1B). The curette is sharply applied to the cartilage with a constant downward twisting motion from superior to inferior. The inferior rim of the cartilage is left intact in a hinged fashion to avoid the creation of a loose body.

   

  An arthroscopic grasper is then used to retrieve the biopsy specimen (TECH FIG 1C,D). Alternative techniques for harvest include use of a small curved osteotome or sharp gouge. If the sample appears insufficient, the biopsy procedure can be repeated in the same location or move to a new location. The cartilage biopsy specimen is then transferred in a sterile fashion to the transport kit. In vitro cell expansion takes 3 to 5 weeks before the cells are available for second-stage implantation.

   

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  TECH FIG 1 • A. The ICRS defect mapping worksheet. (continued)

   

   

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  TECH FIG 1 • (continued) B. Ring curettes for cartilage biopsy. C. Use of a ring curette for articular cartilage biopsy. D. Arthroscopic biopsy of articular cartilage for ACI. (A,B: From Browne JE, Sasser TM, Branch TP. Autologous chondrocyte implantation. Tech Knee Surg 2006;5[4]:238-251.)

• Step 2. Preparation of the Articular Cartilage Lesion

   

  The defect is exposed through an open arthrotomy, allowing for full visualization of the lesion. The defect is then débrided until a healthy cartilage rim is present. A probe can be used to assess the peripheral margins of the lesion for fibrillations and undermined unstable cartilage (TECH FIG 2). A 15-blade scalpel is used to incise the cartilage perpendicular to the surface in order to create a well-shouldered vertical lesion. It is critical to remove all damaged cartilage. The base of the lesion is then carefully scraped with a curette to expose the calcified

   

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  cartilage layer. Care should be taken to avoid penetration of the underlying subchondral bone when débridement of the lesion is performed.

   

   

   

  TECH FIG 2 • A,B. The unstable edges of unhealthy cartilage at the periphery of the lesion are outlined.

  C. The unstable cartilage is excised with a ring curette. D,E. Stable, vertical borders are created to contain the defect. (continued)

   

   

   

  TECH FIG 2 • (continued) F. The lesion is then measured and templated for appropriate sizing. (Courtesy of Genzyme, Inc.)

   

   

  The dimensions of the lesion are then measured in length and width. A template of the lesion is then created by using a marking pen to outline the lesion often using the sterile wrapper from a suture package or glove packaging. The template should be slightly oversized by 2 to 3 mm as the periosteal patch or collagen membrane may shrink slightly during preparation.

• Step 3A. Periosteal Patch Harvest

   

  Through a 4-cm incision in the anteromedial tibia, just below the pes anserinus insertion, the periosteum

  is exposed by gently sweeping away the subcutaneous tissue (TECH FIG 3). The periosteum is shiny white in color. The template is then applied to the periosteum and outlined with a marking pen. The periosteum is then harvested with a 15-blade scalpel and gently removed with a small periosteal elevator. One or two small nontoothed forceps are used to handle the patch to avoid inadvertent penetration of the patch. The patch is then placed in a moist sponge for letter application over the defect. The outer layer of the patch is marked, orienting the patch so the cambium layer faces in toward the lesion.

   

   

   

  TECH FIG 3 • A. The incision for harvest of the periosteal patch is typically 4 cm in length created just below the pes anserinus insertion. B. A small elevator is used to create an edge around the periosteum for harvest. (Courtesy of Genzyme, Inc.)

• Step 3B. Collagen Membrane Preparation

   

  Collagen type I/III membranes such as the Bio-Gide patch (Geistlich Pharma, Wolhusen, Switzerland) have been used in both Europe and United States studies with improved clinical outcomes.8,15,24 The slightly oversized template of the lesion is placed over the collagen membrane and subsequently cut to

  size. The membrane is then soaked in sterile saline in preparation for application over the defect. The

  membrane resorbs completely over several months after application.

• Step 4. Periosteal or Collagen Patch Fixation

   

  Prior to application of the patch, the tourniquet may be released to assess bleeding at the defect site. It is important to prevent bleeding into the defect site to decrease the formation of fibrocartilage from undifferentiated bone marrow mesenchymal stem cells. Bleeding can be controlled with epinephrine-soaked neural patties and/or thrombin gel in the defect. If a periosteal patch has been harvested, the donor site can be closed at this time.

   

  The goals of patch fixation are to provide a watertight membrane to contain the chondrocytes, act as a semipermeable membrane for synovial fluid diffusion to nourish the chondrocytes, and (in the case of periosteal patches) maintain a viable cambium layer to provide growth factors to enhance chondrocyte growth. The cambium layer is oriented toward the subchondral bone.

   

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  The patch is sutured over the defect using dyed 6-0 Vicryl suture (Ethicon, Somerville, NJ) on a P-1 cutting needle. The suture is immersed in mineral oil, allowing the suture to easily pass through the

  periosteum and cartilage. The sutures are passed in an opposing fashion to stretch the patch evenly over the lesion, likened to tightening of a drum (TECH FIG 4 A-C). The sutures are placed through the periosteum first and then through the cartilage. The knots are tied on the side of the patch to avoid friction of the knots against the cartilage with motion and prevent unraveling that may lead to delamination of the patch. Sutures are placed 3 mm apart around the lesion. The superiormost portion of the patch is left open for final placement of the chondrocytes.

   

   

   

  TECH FIG 4 • A. The corners of the periosteal patch are sutured to secure the patch first. B. The needle is placed through the patch first and directed in to the cartilage for a secure bite. C. The knot is tied on the periosteal side to avoid shear of the knot. D. The superior portion of the patch is left open to allow for insertion of the Angiocath to inject the cells. E. Fibrin glue is applied around the periphery of the patch to create a watertight seal. (Courtesy of Genzyme, Inc.)

   

   

  An 18-gauge angiocatheter on a tuberculin syringe filled with saline is injected into the lesion gently under the patch to assess for leakage of fluid around the periphery. Additional sutures may be placed to provide additional patch security. The saline is then reaspirated from the defect. Watertight integrity is further supplemented by using a fibrin sealant such as Tisseel (Baxter Healthcare Corp., Glendale, CA) that is manufactured from pooled human serum. The sealant should be allowed to cure to a more “tacky” consistency prior to application around the periphery of the lesion (TECH FIG 4D,E). The saline test may be repeated as necessary.

• Step 5. Chondrocyte Implantation

   

  The chondrocytes are provided in a culture medium inside a Carticel vial (Genzyme Biosurgery, Cambridge, MA). Care should be taken to maintain sterility of the chondrocytes when aspirating the cells from the vial. Chondrocytes are aspirated using an 18-gauge angiocatheter to prevent damage to the cells (TECH FIG 5A). The vial is held perpendicular to the floor. The angiocatheter is placed below the surface of the diluent but not into the cell-containing plug at the bottom of the vial. The cells are then gently aspirated and resuspended multiple times. The angiocatheter and tuberculin syringe containing the suspended chondrocytes is then inserted through the window in the patch, slowly filling the defect.

  The superior window is then closed with suture and fibrin glue to seal in the chondrocytes (TECH FIG 5B,C). The incision site is then irrigated and the arthrotomy is closed in a layered fashion. A drain is typically not used to avoid inadvertent injury to the patch.

   

   

   

  TECH FIG 5 • A. The chondrocytes are aspirated in a sterile fashion from the vial. B,C. Lateral femoral condyle lesion before (B) and after (C) completion of ACI after injection of cells into the defect.

   

   

   

• Special Considerations

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In the setting where a defect is not contained with a healthy cartilage rim, several options are available to secure the patch. Suturing the patch to adjacent synovium or through drill holes in the bone may be used. The authors used small absorbable suture anchors spaced 3 to 4 mm apart to provide points of fixation for the patch.

 

Patella and femoral trochlea lesions result in a lesion that is convex or concave, making patch placement over the defect challenging. The patch should be oversized in these situations. The first sutures should be placed at the central median ridge superior and inferior to the lesion likened to “pitching a tent.” The sutures are then placed around the remainder of the lesion in a similar fashion as standard lesions.

 

In patients with an articular cartilage lesion in which the osseous defect is more than 8 to 10 mm in depth, bone grafting may be necessary first prior to proceeding with ACI. The bone graft may be performed at the time of the initial articular cartilage biopsy. A 6- to 9-month interval is recommended prior to staged chondrocyte implantation to ensure the subchondral plate integrity has been established. Another option to treat osseous defects is the “sandwich technique” where the defect is bone grafted and sealed with a

periosteal patch, cambium layer facing up.17 The ACI is then performed over the top with an additional periosteal patch in the standard fashion.

 

PEARLS AND PITFALLS

Pearls ▪ Correct concomitant ligamentous instability, meniscal pathology (including allograft

transplantation), and/or limb malalignment prior to ACI.

• Leave a hinge of articular cartilage intact after harvest with the ring curette to prevent creation of a loose body.

• Remove all nonviable or damaged articular cartilage from the periphery of the lesion.

• Avoid penetration of the subchondral plate during débridement of the base of the defect.

• Slightly oversize the periosteal or collagen patch by 2-3 mm to avoid undercoverage of

 

 

	the defect. Tie sutures on the patch side of the lesion to avoid knot abrasion or delamination of the patch. Sterile harvest of the chondrocytes from the vial with an 18-gauge angiocatheter should be done to avoid injury to chondrocytes. Assess for a watertight seal of the patch to ensure containment of the chondrocytes in the defect. Patients are counseled pre- and postoperatively to the risk of recurrent injury during high-impact sporting activities. Use of an unloader brace postoperatively may be beneficial in some cases.

 

 

 

POSTOPERATIVE CARE

 

Postoperative rehabilitation protocols following ACI rely on a slow, gradual course allowing maturation of the transplanted chondrocytes. Protection of the cartilage tissue from excessive forces prevents delamination of the patch and safe restoration of early range of motion. Four phases of rehabilitation have been outlined

coinciding with the biologic phases of healing that occur after ACI.2,4,17,18

 

First phase is the proliferation-protection phase that lasts the first 6 weeks postoperative. A continuous passive motion (CPM) is initiated 12 to 24 hours postoperative allowing the cells to become adherent to the bond surface. The CPM is used 6 to 8 hours per day during this phase. Non- or toetouch weight bearing using crutches is continued until quadriceps strength and full range of motion is restored. Gradual progression to full weight bearing with a normal gait may take 10 to 12 weeks. In patellofemoral ACI procedures, the CPM is limited to 40 degrees the first 2 to 3 weeks followed by gradual progression. Pool therapy may be initiated at 4

to 6 weeks, allowing for the buoyancy effect of water to assist partial weight bearing.4

 

Second phase is the transitional-protective phase between weeks 7 and 12. Patients are allowed to resume normal activities of daily living. In some instances of isolated medial or lateral femoral lesions, an unloader brace has been used to further protect the surgical site.

 

Third phase is the remodeling-functional phase from weeks 12 to 32. A progressive walking program is initiated with advancement to elliptical, swimming, and cycling. Squatting, kneeling, and jumping should be avoided until the patient can perform all lower extremity resistance activities with little pain, inflammation, or effusion.

 

Final phase, the maturation phase, may take 18 to 24 months after implantation. In general, jogging and aerobics can be performed at 9 to 12 months. High-impact sports are allowed at 12 to 18 months.

 

OUTCOMES

Minas et al17 recently reported outcomes with a minimum 10-year follow-up after first-generation ACI. Survivorship of 71% and improved function in 75% of patients was reported. A history of prior

microfracture and larger sized defects were associated with an increased risk of failure. Niemeyer et al21 reported a mean follow-up of 10 years in 70 patients treated with first-generation ACI. Seventy-seven percent of patients reported being “satisfied” with the outcome.

Goyal et al9 published a systematic review of level I and II studies of second- and third-generation ACI compared to first-generation techniques. There was weak evidence showing that collagen membrane-

 

 

based ACI resulted in better clinical outcomes than periosteum-based ACI. Gomoll et al8 reported a multicenter cohort of 300 patients treated either

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with a collagen type I/III membrane or periosteum-based ACI. At 1-year follow-up, the rate of reoperation for graft hypertrophy was 25.7% in the periosteum group and 5% in the collagen membrane group.

Failure rates were similar, 2.3% to 4%, between groups. Decreased overall cost has been demonstrated using collagen type I/III membrane ACI versus periosteal patch ACI.5,24 McCarthy and Roberts15 reported

results of 88 patients treated either with collagen membrane-based ACI or periosteum-based ACI.15 Postoperative biopsies were taken at a mean of 16 to 19 months postoperative. Compared with periosteum-based ACI, the repair tissue formed from patients treated with collagen membrane-based ACI demonstrated a significantly higher score for cellular morphology and higher proportion of hyaline cartilage formation. Both groups exhibited a significant increase in Lysholm score post-ACI.

Harris et al10 performed a systematic review of 13 level I and II studies comparing ACI to other cartilage repair or restoration techniques. All surgical techniques studied demonstrated improvement in comparison with the preoperative status. Three of 7 studies showed better clinical outcomes after ACI in comparison with microfracture with an average of 1 to 3 years follow-up. ACI and osteochondral autograft demonstrated equivalent short-term clinical outcomes. Outcomes were equivalent between first- and second-generation ACI. Complication rates were higher for periosteal patch first-generation ACI. Younger patients with a shorter preoperative duration of symptoms and fewer prior surgical procedures had the

best outcomes after ACI or microfracture. A defect size of greater than 4 cm2 was the only factor predictive of better outcomes when ACI was compared with a non-ACI surgical technique.

 

COMPLICATIONS

Common complications after ACI include prolonged postoperative effusion, adhesions/arthrofibrosis, synovitis, hypertrophy of the periosteal patch, delamination of the graft, and donor site morbidity.

A reoperation rate after first-generation periosteal patch ACI has been reported in as many as 50% of cases.1,8,9,14,17,18,23 The majority of reoperations are for periosteal patch hypertrophy causing persistent mechanical symptoms.

A persistent effusion and mechanical symptoms are frequent 3 to 7 months postoperatively. Most often, these symptoms spontaneously resolve.

Arthroscopic débridement of patch hypertrophy can be performed for persistent mechanical symptoms that do not resolve over time.

Gomoll et al8 reported a decrease in the rate of reoperation for graft hypertrophy with the use of a collagen type I/III membrane from 25.7% to 5%.

 

 

REFERENCES

1. Bedi A, Feeley BT, Williams RJ III. Management of articular cartilage defects of the knee. J Bone Joint Surg Am 2010;92(4):994-1009.

    

    

2. Brittberg M, Lindahl A, Nilsson A, et al. Treatment of deep cartilage defects in the knee with autologous

   chondrocyte transplantation. N Engl J Med 1994;331(14):889-895.

    

    

3. Browne JE, Branch TP. Surgical alternatives for treatment of articular cartilage lesions. J Am Acad Orthop Surg 2000;8(3):180-189.

    

    

4. Browne JE, Sasser TM, Branch TP. Autologous chondrocyte implantation. Tech Knee Surg 2006;5(4):238-251.

    

    

5. Donohue JM, Buss D, Oegema TR Jr, et al. The effects of indirect blunt trauma on adult canine articular cartilage. J Bone Joint Surg Am 1983;65(7):948-957.

    

    

6. Elsaid KA, Zhang L, Waller K, et al. The impact of forced joint exercise on lubricin biosynthesis from articular cartilage following ACL transection and intra-articular lubricin's effect in exercised joints following ACL transection. Osteoarthritis Cartilage 2012;20(8):940-948.

    

    

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